Bult H, Fret H R, Herman A G
Division of Pharmacology, University of Antwerp (UIA), Wilrijk, Belgium.
J Cardiovasc Pharmacol. 1989;14 Suppl 11:S120-3.
SIN-1, the metabolite of molsidomine, caused a dose-dependent inhibition of the aggregation of rabbit platelets induced by adenosine diphosphate (ADP) and the stable thromboxane mimetic U-46619. Molsidomine was inactive in this respect. In the presence of a threshold concentration of prostacyclin, the antiaggregating activity of SIN-1 became more pronounced. As a result, the dose-response curve of SIN-1 was shifted to the left. These findings suggest that SIN-1 could be of therapeutic value to suppress platelet aggregation during atherosclerotic disease when the endogenous supply of endothelium-derived relaxing factor is compromised.
硝普钠（SIN-1）是吗多明的代谢产物，它能剂量依赖性地抑制二磷酸腺苷（ADP）和稳定的血栓素类似物U-46619诱导的兔血小板聚集。吗多明在这方面无活性。在存在阈值浓度前列环素的情况下，SIN-1的抗聚集活性变得更加明显。结果，SIN-1的剂量反应曲线向左移动。这些发现表明，当内皮源性舒张因子的内源性供应受损时，SIN-1在抑制动脉粥样硬化疾病期间的血小板聚集方面可能具有治疗价值。
